Indian Journal of Critical Care Medicine November 2014 Vol 18 Issue 11
of acute respiratory failure used by the authors includes subjective terms such as “moderate to severe dyspnea” and “moderate to severe acidosis” and it has not been clarified whether rigid criteria (e.g. Arterial blood gas) as used by other studies[2,3] has been adhered to. Due to this it may be difficult to generalize the results of this study as the practice might vary from one physician/institute to the other II Some indications of NIV use as mentioned by the authors need further explanation. Around 13 cases of nonpulmonary sepsis received NIV (they were not in the acute lung injury/acute respiratory distress syndrome [ARDS] group), but the pathophysiology addressed by NIV was not clear. Similarly, two patients with gastro‑intestinal bleed received NIV (who probably did not have severe gastro‑intestinal symptoms or aspiration as it was a contraindication in the present study), but still had “acute respiratory failure” necessitating NIV administration. A patient with pleural effusion also received NIV, but the reason for the same has not been elucidated. It might seem that in the absence of strict guidelines to initiate NIV there may have left scope for the “overdoing” – a question which the authors themselves ask in the title III The authors hypothesize that the reason for higher rate of NIV failure in group 2 could be due to longer period of observation in these cases, as per the data provided by Purwar et al., the differences between the number of patients who were intubated within 2 h or after 2 h were not significant in this study. It can be difficult to pinpoint the reason for more deaths in group 2, but it seems that use of NIV is addresses the pathophysiology more effectively for group 1 than for group 2 indications that is, say it works better for acute exacerbation of chronic obstructive pulmonary disease than in cases of ARDS. While reverses the hypoventilation in the former while it is not as effective as invasive ventilation for recruiting the lung units in the latter. Anyway as per evidence it seems more logical to have a lower threshold for conversion to invasive ventilation in cases of nonlevel 1 indications as in these cases the evidence is less robust and the chance of failure are higher.
Animesh Ray
Department of Pulmonary Critical Care and Sleep Medicine, VMMC and Safdarjang Hospital, New Delhi, India
Correspondence: Dr. Animesh Ray,Department of Pulmonary Critical Care and Sleep Medicine, VMMC and Safdarjang Hospital, New Delhi, India E‑mail: [email protected]
References 1.
Purwar S, Venkataraman R, Senthilkumar R, Ramakrishnan N,
2.
3.
Abraham BK. Noninvasive ventilation: Are we overdoing it? Indian J Crit Care Med 2014;18:503‑7. Agarwal R, Handa A, Aggarwal AN, Gupta D, Behera D. Outcomes of noninvasive ventilation in acute hypoxemic respiratory failure in a respiratory intensive care unit in north India. Respir Care 2009;54:1679‑87. Carrillo A, Gonzalez‑Diaz G, Ferrer M, Martinez‑Quintana ME, Lopez‑Martinez A, Llamas N, et al. Non‑invasive ventilation in community‑acquired pneumonia and severe acute respiratory failure. Intensive Care Med 2012;38:458‑66.
Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.144028
Intensive care unit management of a posttraumatic pneumonectomy case Sir, Tracheobronchial rupture following blunt chest trauma is rare and life‑threatening. Surgical repair is done in most cases and pneumonectomy is avoided whenever possible as emergency pneumonectomy carries high mortality rate of 50-70%.[1] This is due to contributory effects of hypotension, hypoxia and abrupt rise in pulmonary vascular resistance leading to right ventricular failure[2] and so postoperative care in intensive care unit (ICU) is very important. We describe ICU management of such a case. An 18‑year‑old male of chest trauma presented to the emergency referred from another hospital. Vitals were pulse 113/min, blood pressure 152/82 mmHg, respiratory rate (RR) 35/min, saturation 84% with massive subcutaneous emphysema and intercostal chest drain (ICD) in situ. Patient was immediately intubated, and another ICD inserted on the right side. Chest X‑ray (CXR) post ICD revealed massive pneumothorax on right side [Figure 1]. Computed tomography chest revealed complete transection of right main bronchus. Patient was shifted to emergency operation theatre and intubated with double lumen tube (DLT). Intraoperatively as bronchial anastomosis was 763
Indian Journal of Critical Care Medicine November 2014 Vol 18 Issue 11
Figure 1: Preoperative chest X-ray of patient showing collapsed lung with intercostal chest drain in situ
Figure 2: Postoperative chest X-ray showing left sided double lumen endotracheal tube
not possible, right sided pneumonectomy was done, and patient was shifted to the ICU. In the ICU, instead of changing to a single lumen tube, we ventilated the patient with DLT [Figure 2] only for 12 h as there were high chances of bronchial stump rupture. Patient was kept on volume control with a tidal volume 5 ml/kg, positive end expiratory pressure (PEEP) of 5 cm H2O, with respiratory rate (RR) adjusted to limit plateau airway pressure to 20 cm H2O. PaCO2 50-55 mmHg was accepted. Fluid intake was restricted to maintain urine output >0.5 ml/kg/h. Weaning was started after 24 h and patient extubated on the 3rd postoperative day and put on noninvasive ventilation (NIV) intermittently for the next 2 days. CXR was done daily to monitor the fluid in postpneumonectomy space (PPS). With active physiotherapy and mobilization, patient did well and was discharged from ICU on 9th postoperative day [CXR, Figure 3] and from the hospital on 14th day. At the time of discharge, he could climb two flights of stairs without dyspnea. The common causes of early postoperative death after emergency pneumonectomy are bleeding, postpneumonectomy pulmonary edema, right ventricular failure and arrhythmias, [2] risk factors being increased age, higher injury severity score, right sided pneumonectomy and comorbid condition. [3] The incidence of pulmonary edema is higher for right pneumonectomy but can be avoided with judicious fluid management. We maintained a negative fluid balance of 500 ml/24 h. Radiographic monitoring of PPS is crucial. Immediately after surgery PPS fills with air.[4] Then, fluid accumulates at a rate of two rib spaces per day and 80-90% is filled in 2 weeks. If fluid accumulates more rapidly, then possibility of hemorrhage, infection or chylothorax should be kept in mind. Arrythmias are seen in 9-34% patients, mainly in advanced age group.[5] After pneumonectomy work of breathing increases so patient remains tachypenic. We kept our patient on NIV intermittently and accepted an RR of 25-30/min. In conclusion, adequate knowledge about changes postpneumonectomy and management of complications are vital for a favorable outcome.
Richa Aggarwal, Deviprasad Dash, Kapil Dev Soni, Biplab Mishra1
Department of Critical Care Medicine and 1Surgery, JPNA Trauma Centre, AIIMS, New Delhi, India
Figure 3: Chest X-ray on 8th postoperative day showing postpneumonectomy space filled with fluid 764
Correspondence: Dr. Richa Aggarwal, Departments of Critical Care Medicine, JPNA Trauma Centre, AIIMS, New Delhi ‑ 110 029, India. E‑mail: [email protected]
Indian Journal of Critical Care Medicine November 2014 Vol 18 Issue 11
References 1. 2. 3. 4. 5.
Tominaga GT, Waxman K, Scannell G, Annas C, Ott RA, Gazzaniga AB. Emergency thoracotomy with lung resection following trauma. Am Surg 1993;59:834‑7. Klein Y, Kishinevsky E, Konichezky S, Bregman G, Klein M, Kashtan H. Postoperative management after pneumonectomy for blunt thoracic trauma. Eur J Trauma Emerg Surg 2007;33:422‑4. Kopec SE, Irwin RS, Umali‑Torres CB, Balikian JP, Conlan AA. The postpneumonectomy state. Chest 1998;114:1158‑84. Spirn PW, Gross GW, Wechsler RJ, Steiner RM. Radiology of the chest after thoracic surgery. Semin Roentgenol 1988;23:9‑31. Harpole DH, Liptay MJ, DeCamp MM Jr, Mentzer SJ, Swanson SJ, Sugarbaker DJ. Prospective analysis of pneumonectomy: Risk factors for major morbidity and cardiac dysrhythmias. Ann Thorac Surg 1996;61:977‑82.
use.[5] The nutritional problem seems to be an important factor leading to hypomagnesemia.[4,5] Hence, finding of hypomagnesemia in the patient receiving PPI might not imply that PPI is the cause of the problem. Finally, the routine electrolyte investigation usually does not cover serum magnesium. Hence, the problem might be underor late-diagnosed. Critical care unit practitioners should regularly monitor the serum magnesium of the patient to detect the problem early.[6]
Sim Sai Tin, Viroj Wiwanitkit1
Medical Center, Shantou, 1Hainan Medical University, Haikou, China
Correspondence: Prof. Sim Sai Tin, Medical Center, Shantou, China. E‑mail: [email protected]
Access this article online Quick Response Code:
Website: www.ijccm.org
References 1.
DOI: 10.4103/0972-5229.144029
2. 3.
Symptomatic hypomagnesemia and proton pump inhibitors
4. 5. 6.
Wang AK, Sharma S, Kim P, Mrejen‑Shakin K. Hypomagnesemia in the intensive care unit: Choosing your gastrointestinal prophylaxis, a case report and review of the literature. Indian J Crit Care Med 2014;18:456‑60. Mackay JD, Bladon PT. Hypomagnesaemia due to proton‑pump inhibitor therapy: A clinical case series. QJM 2010;103:387‑95. Ströker E, Leone L, Vandeput Y, Borbath I, Lefebvre C. Severe symptomatic hypomagnesaemia induced by the chronic use of proton pump inhibitors: A case report of a patient with Zollinger‑Ellison syndrome. Acta Clin Belg 2014;69:62‑5. Ayuk J, Gittoes NJ. How should hypomagnesaemia be investigated and treated? Clin Endocrinol (Oxf) 2011;75:743‑6. Deshmukh CT, Rane SA, Gurav MN. Hypomagnesaemia in paediatric population in an intensive care unit. J Postgrad Med 2000;46:179‑80. Centeno C, López Saca JM. An update on the importance of monitoring serum magnesium in advanced disease patients. Curr Opin Support Palliat Care 2013;7:396‑405. Access this article online
Sir, We read with interest the report by [1] Wang et al. titled “a case of symptomatic hypomagnesaemia in medical intensive care unit that is strongly related to PPIs”.[1] In fact, symptomatic hypomagnesemia and PPI is sporadically mentioned. In the case series by Mackay and Bladon the problem is common among the elderly with long‑term use of PPI, and the stopping of PPI can dramatically improve the problem.[2] Of interest, not all patients receiving PPI develop symptomatic hypomagnesemia. The possible relationship to a serious disease, Zollinger–Ellison syndrome, is mentioned.[3] Focusing on the present report, the case in intensive care context is reported. The problem of hypomagnesemia is not an extremely rare condition. As noted by Ayuk and Gittoes, “hypomagnesaemia is relatively common, with an estimated prevalence in the general population ranging from 2.5% to 15%”[4] and this can be due to many factors, not specific to use of PPI. In addition, according to a report by Deshmukh et al., 70% of patients in critical care unit had hypomagnesemia, despite no history of PPI
Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.144030
Refractory hyperkalemia related to heparin abuse Sir, We read with interest the case report of refractory hyperkalemia due to heparin abuse. [1] An effect of heparin is hypoaldosteronism with hyperkalemia caused by direct inhibition of aldosterone biosynthesis 765
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
of acute respiratory failure used by the authors includes subjective terms such as “moderate to severe dyspnea” and “moderate to severe acidosis” and it has not been clarified whether rigid criteria (e.g. Arterial blood gas) as used by other studies[2,3] has been adhered to. Due to this it may be difficult to generalize the results of this study as the practice might vary from one physician/institute to the other II Some indications of NIV use as mentioned by the authors need further explanation. Around 13 cases of nonpulmonary sepsis received NIV (they were not in the acute lung injury/acute respiratory distress syndrome [ARDS] group), but the pathophysiology addressed by NIV was not clear. Similarly, two patients with gastro‑intestinal bleed received NIV (who probably did not have severe gastro‑intestinal symptoms or aspiration as it was a contraindication in the present study), but still had “acute respiratory failure” necessitating NIV administration. A patient with pleural effusion also received NIV, but the reason for the same has not been elucidated. It might seem that in the absence of strict guidelines to initiate NIV there may have left scope for the “overdoing” – a question which the authors themselves ask in the title III The authors hypothesize that the reason for higher rate of NIV failure in group 2 could be due to longer period of observation in these cases, as per the data provided by Purwar et al., the differences between the number of patients who were intubated within 2 h or after 2 h were not significant in this study. It can be difficult to pinpoint the reason for more deaths in group 2, but it seems that use of NIV is addresses the pathophysiology more effectively for group 1 than for group 2 indications that is, say it works better for acute exacerbation of chronic obstructive pulmonary disease than in cases of ARDS. While reverses the hypoventilation in the former while it is not as effective as invasive ventilation for recruiting the lung units in the latter. Anyway as per evidence it seems more logical to have a lower threshold for conversion to invasive ventilation in cases of nonlevel 1 indications as in these cases the evidence is less robust and the chance of failure are higher.
Animesh Ray
Department of Pulmonary Critical Care and Sleep Medicine, VMMC and Safdarjang Hospital, New Delhi, India
Correspondence: Dr. Animesh Ray,Department of Pulmonary Critical Care and Sleep Medicine, VMMC and Safdarjang Hospital, New Delhi, India E‑mail: [email protected]
References 1.
Purwar S, Venkataraman R, Senthilkumar R, Ramakrishnan N,
2.
3.
Abraham BK. Noninvasive ventilation: Are we overdoing it? Indian J Crit Care Med 2014;18:503‑7. Agarwal R, Handa A, Aggarwal AN, Gupta D, Behera D. Outcomes of noninvasive ventilation in acute hypoxemic respiratory failure in a respiratory intensive care unit in north India. Respir Care 2009;54:1679‑87. Carrillo A, Gonzalez‑Diaz G, Ferrer M, Martinez‑Quintana ME, Lopez‑Martinez A, Llamas N, et al. Non‑invasive ventilation in community‑acquired pneumonia and severe acute respiratory failure. Intensive Care Med 2012;38:458‑66.
Access this article online Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.144028
Intensive care unit management of a posttraumatic pneumonectomy case Sir, Tracheobronchial rupture following blunt chest trauma is rare and life‑threatening. Surgical repair is done in most cases and pneumonectomy is avoided whenever possible as emergency pneumonectomy carries high mortality rate of 50-70%.[1] This is due to contributory effects of hypotension, hypoxia and abrupt rise in pulmonary vascular resistance leading to right ventricular failure[2] and so postoperative care in intensive care unit (ICU) is very important. We describe ICU management of such a case. An 18‑year‑old male of chest trauma presented to the emergency referred from another hospital. Vitals were pulse 113/min, blood pressure 152/82 mmHg, respiratory rate (RR) 35/min, saturation 84% with massive subcutaneous emphysema and intercostal chest drain (ICD) in situ. Patient was immediately intubated, and another ICD inserted on the right side. Chest X‑ray (CXR) post ICD revealed massive pneumothorax on right side [Figure 1]. Computed tomography chest revealed complete transection of right main bronchus. Patient was shifted to emergency operation theatre and intubated with double lumen tube (DLT). Intraoperatively as bronchial anastomosis was 763
Indian Journal of Critical Care Medicine November 2014 Vol 18 Issue 11
Figure 1: Preoperative chest X-ray of patient showing collapsed lung with intercostal chest drain in situ
Figure 2: Postoperative chest X-ray showing left sided double lumen endotracheal tube
not possible, right sided pneumonectomy was done, and patient was shifted to the ICU. In the ICU, instead of changing to a single lumen tube, we ventilated the patient with DLT [Figure 2] only for 12 h as there were high chances of bronchial stump rupture. Patient was kept on volume control with a tidal volume 5 ml/kg, positive end expiratory pressure (PEEP) of 5 cm H2O, with respiratory rate (RR) adjusted to limit plateau airway pressure to 20 cm H2O. PaCO2 50-55 mmHg was accepted. Fluid intake was restricted to maintain urine output >0.5 ml/kg/h. Weaning was started after 24 h and patient extubated on the 3rd postoperative day and put on noninvasive ventilation (NIV) intermittently for the next 2 days. CXR was done daily to monitor the fluid in postpneumonectomy space (PPS). With active physiotherapy and mobilization, patient did well and was discharged from ICU on 9th postoperative day [CXR, Figure 3] and from the hospital on 14th day. At the time of discharge, he could climb two flights of stairs without dyspnea. The common causes of early postoperative death after emergency pneumonectomy are bleeding, postpneumonectomy pulmonary edema, right ventricular failure and arrhythmias, [2] risk factors being increased age, higher injury severity score, right sided pneumonectomy and comorbid condition. [3] The incidence of pulmonary edema is higher for right pneumonectomy but can be avoided with judicious fluid management. We maintained a negative fluid balance of 500 ml/24 h. Radiographic monitoring of PPS is crucial. Immediately after surgery PPS fills with air.[4] Then, fluid accumulates at a rate of two rib spaces per day and 80-90% is filled in 2 weeks. If fluid accumulates more rapidly, then possibility of hemorrhage, infection or chylothorax should be kept in mind. Arrythmias are seen in 9-34% patients, mainly in advanced age group.[5] After pneumonectomy work of breathing increases so patient remains tachypenic. We kept our patient on NIV intermittently and accepted an RR of 25-30/min. In conclusion, adequate knowledge about changes postpneumonectomy and management of complications are vital for a favorable outcome.
Richa Aggarwal, Deviprasad Dash, Kapil Dev Soni, Biplab Mishra1
Department of Critical Care Medicine and 1Surgery, JPNA Trauma Centre, AIIMS, New Delhi, India
Figure 3: Chest X-ray on 8th postoperative day showing postpneumonectomy space filled with fluid 764
Correspondence: Dr. Richa Aggarwal, Departments of Critical Care Medicine, JPNA Trauma Centre, AIIMS, New Delhi ‑ 110 029, India. E‑mail: [email protected]
Indian Journal of Critical Care Medicine November 2014 Vol 18 Issue 11
References 1. 2. 3. 4. 5.
Tominaga GT, Waxman K, Scannell G, Annas C, Ott RA, Gazzaniga AB. Emergency thoracotomy with lung resection following trauma. Am Surg 1993;59:834‑7. Klein Y, Kishinevsky E, Konichezky S, Bregman G, Klein M, Kashtan H. Postoperative management after pneumonectomy for blunt thoracic trauma. Eur J Trauma Emerg Surg 2007;33:422‑4. Kopec SE, Irwin RS, Umali‑Torres CB, Balikian JP, Conlan AA. The postpneumonectomy state. Chest 1998;114:1158‑84. Spirn PW, Gross GW, Wechsler RJ, Steiner RM. Radiology of the chest after thoracic surgery. Semin Roentgenol 1988;23:9‑31. Harpole DH, Liptay MJ, DeCamp MM Jr, Mentzer SJ, Swanson SJ, Sugarbaker DJ. Prospective analysis of pneumonectomy: Risk factors for major morbidity and cardiac dysrhythmias. Ann Thorac Surg 1996;61:977‑82.
use.[5] The nutritional problem seems to be an important factor leading to hypomagnesemia.[4,5] Hence, finding of hypomagnesemia in the patient receiving PPI might not imply that PPI is the cause of the problem. Finally, the routine electrolyte investigation usually does not cover serum magnesium. Hence, the problem might be underor late-diagnosed. Critical care unit practitioners should regularly monitor the serum magnesium of the patient to detect the problem early.[6]
Sim Sai Tin, Viroj Wiwanitkit1
Medical Center, Shantou, 1Hainan Medical University, Haikou, China
Correspondence: Prof. Sim Sai Tin, Medical Center, Shantou, China. E‑mail: [email protected]
Access this article online Quick Response Code:
Website: www.ijccm.org
References 1.
DOI: 10.4103/0972-5229.144029
2. 3.
Symptomatic hypomagnesemia and proton pump inhibitors
4. 5. 6.
Wang AK, Sharma S, Kim P, Mrejen‑Shakin K. Hypomagnesemia in the intensive care unit: Choosing your gastrointestinal prophylaxis, a case report and review of the literature. Indian J Crit Care Med 2014;18:456‑60. Mackay JD, Bladon PT. Hypomagnesaemia due to proton‑pump inhibitor therapy: A clinical case series. QJM 2010;103:387‑95. Ströker E, Leone L, Vandeput Y, Borbath I, Lefebvre C. Severe symptomatic hypomagnesaemia induced by the chronic use of proton pump inhibitors: A case report of a patient with Zollinger‑Ellison syndrome. Acta Clin Belg 2014;69:62‑5. Ayuk J, Gittoes NJ. How should hypomagnesaemia be investigated and treated? Clin Endocrinol (Oxf) 2011;75:743‑6. Deshmukh CT, Rane SA, Gurav MN. Hypomagnesaemia in paediatric population in an intensive care unit. J Postgrad Med 2000;46:179‑80. Centeno C, López Saca JM. An update on the importance of monitoring serum magnesium in advanced disease patients. Curr Opin Support Palliat Care 2013;7:396‑405. Access this article online
Sir, We read with interest the report by [1] Wang et al. titled “a case of symptomatic hypomagnesaemia in medical intensive care unit that is strongly related to PPIs”.[1] In fact, symptomatic hypomagnesemia and PPI is sporadically mentioned. In the case series by Mackay and Bladon the problem is common among the elderly with long‑term use of PPI, and the stopping of PPI can dramatically improve the problem.[2] Of interest, not all patients receiving PPI develop symptomatic hypomagnesemia. The possible relationship to a serious disease, Zollinger–Ellison syndrome, is mentioned.[3] Focusing on the present report, the case in intensive care context is reported. The problem of hypomagnesemia is not an extremely rare condition. As noted by Ayuk and Gittoes, “hypomagnesaemia is relatively common, with an estimated prevalence in the general population ranging from 2.5% to 15%”[4] and this can be due to many factors, not specific to use of PPI. In addition, according to a report by Deshmukh et al., 70% of patients in critical care unit had hypomagnesemia, despite no history of PPI
Quick Response Code:
Website: www.ijccm.org
DOI: 10.4103/0972-5229.144030
Refractory hyperkalemia related to heparin abuse Sir, We read with interest the case report of refractory hyperkalemia due to heparin abuse. [1] An effect of heparin is hypoaldosteronism with hyperkalemia caused by direct inhibition of aldosterone biosynthesis 765
Copyright of Indian Journal of Critical Care Medicine is the property of Medknow Publications & Media Pvt. Ltd. and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use.
